Blunted Cardiac Output from Overtraining Is Related to Increased Arterial Stiffness

Moderate overtraining has been characterized by decreased exercising HR and recently decreased exercising stroke volume (SV), independent of alterations to blood volume. The aim of this study was to assess changes in arterial stiffness and central hemodynamics, and their relationship to exercising SV, after 3 wk of overload training.

Twenty-six cyclists and triathletes completed 3 wk of either regular training (CON; n = 13) or overload training (OL; n = 13). Testing took place before (PRE) and after regular or overload training (POST). Resting measures included brachial blood pressure, HR, carotid-femoral pulse wave velocity (PWV) to assess arterial stiffness, and carotid pulse wave analysis to assess wave reflections and central hemodynamics. An incremental cycle test was used to assess peak power, maximal HR, and maximal lactate to assess overtraining status. Cardiac output (Q˙), SV, and HR were assessed using cardiac impedance.

Resting arterial stiffness was unaltered in CON but increased with OL after increased training (CON -0.1 ± 0.6 m·s vs OL +0.5 ± 0.8 m·s, P = 0.04). Resting blood pressure and central hemodynamics, including aortic pressures, augmentation index, and subendocardial viability ratio, did not change (all P > 0.05). Maximal SV (CON +3 mL vs OL -9 mL, P = 0.04), HR (CON -2 ± 4 bpm vs OL -9 ± 3 bpm, P < 0.001), and Q˙ (CON +0.32 L·min vs OL -1.75 L·min, P = 0.01) decreased with OL from PRE to POST. A significant inverse relationship existed between changes in PWV and maximal Q˙ (r = -0.44, P = 0.04) and changes in PWV and peak power (r = -0.48, P = 0.01), and trended for SV and PWV (r = -0.41, P = 0.055).

Overload training results in increased resting arterial stiffness and reduced SV during exercise, with no changes to resting central hemodynamics.